Catalog Update01 - International Update 31/01/2013 08:18 Page 1
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Strategies to Increase ß-Cell Mass Expansion
This electronic thesis or dissertation has been downloaded from the King’s Research Portal at https://kclpure.kcl.ac.uk/portal/ Strategies to increase -cell mass expansion Drynda, Robert Lech Awarding institution: King's College London The copyright of this thesis rests with the author and no quotation from it or information derived from it may be published without proper acknowledgement. END USER LICENCE AGREEMENT Unless another licence is stated on the immediately following page this work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International licence. https://creativecommons.org/licenses/by-nc-nd/4.0/ You are free to copy, distribute and transmit the work Under the following conditions: Attribution: You must attribute the work in the manner specified by the author (but not in any way that suggests that they endorse you or your use of the work). Non Commercial: You may not use this work for commercial purposes. No Derivative Works - You may not alter, transform, or build upon this work. Any of these conditions can be waived if you receive permission from the author. Your fair dealings and other rights are in no way affected by the above. Take down policy If you believe that this document breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. Download date: 02. Oct. 2021 Strategies to increase β-cell mass expansion A thesis submitted by Robert Drynda For the degree of Doctor of Philosophy from King’s College London Diabetes Research Group Division of Diabetes & Nutritional Sciences Faculty of Life Sciences & Medicine King’s College London 2017 Table of contents Table of contents ................................................................................................. -
Single Dose of the CXCR4 Antagonist BL-8040 Induces Rapid
Published OnlineFirst August 23, 2017; DOI: 10.1158/1078-0432.CCR-16-2919 Cancer Therapy: Clinical Clinical Cancer Research Single Dose of the CXCR4 Antagonist BL-8040 Induces Rapid Mobilization for the Collection of Human CD34þ Cells in Healthy Volunteers Michal Abraham1, Yaron Pereg2, Baruch Bulvik1, Shiri Klein3, Inbal Mishalian3, Hana Wald1, Orly Eizenberg1, Katia Beider4, Arnon Nagler4, Rottem Golan2, Abi Vainstein2, Arnon Aharon2, Eithan Galun3, Yoseph Caraco5, Reuven Or6, and Amnon Peled3,4 Abstract Purpose: The potential of the high-affinity CXCR4 antagonist systemic reactions were mitigated by methylprednisolone, BL-8040 as a monotherapy-mobilizing agent and its derived paracetamol, and promethazine pretreatment. In the first part graft composition and quality were evaluated in a phase I clinical of the study, BL-8040 triggered rapid and substantial mobili- þ study in healthy volunteers (NCT02073019). zation of WBCs and CD34 cells in all tested doses. Four hours Experimental Design: The first part of the study was a ran- postdose, the count rose to a mean of 8, 37, 31, and 35 cells/mL domized, double-blind, placebo-controlled dose escalation (placebo, 0.5, 0.75, and 1 mg/kg, respectively). FACS analysis phase. The second part of the study was an open-label phase, in revealed substantial mobilization of immature dendritic, T, B, þ which 8 subjects received a single injection of BL-8040 (1 mg/kg) and NK cells. In the second part, the mean CD34 cells/kg and approximately 4 hours later underwent a standard leukapher- collected were 11.6 Â 106 cells/kg. The graft composition was esis procedure. -
Inhibition of 50-Khz Ultrasonic Vocalizations by Dopamine Receptor Subtype-Selective Agonists and Antagonists in Adult Rats
Psychopharmacology (2013) 226:589–600 DOI 10.1007/s00213-012-2931-6 ORIGINAL INVESTIGATION Inhibition of 50-kHz ultrasonic vocalizations by dopamine receptor subtype-selective agonists and antagonists in adult rats Tina Scardochio & Paul B. S. Clarke Received: 6 September 2012 /Accepted: 13 November 2012 /Published online: 29 November 2012 # Springer-Verlag Berlin Heidelberg 2012 Abstract calling. The D4 agonist and antagonist did not significantly Rationale Adult rats emit ultrasonic calls at around 22 and affect 50-kHz call rates. Twenty-two-kilohertz calls oc- 50 kHz, which are often elicited by aversive and rewarding curred infrequently under all drug conditions. stimuli, respectively. Dopamine (DA) plays a role in aspects Conclusion Following systemic drug administration, tonic of both reward and aversion. pharmacological activation of D1-like or D2-like DA recep- Objective The purpose of this study is to investigate the tors, either alone or in combination, does not appear suffi- effects of DA receptor subtype-selective agonists on 22- cient to induce 50-kHz calls. Dopaminergic transmission and 50-kHz call rates. through D1, D2, and D3 receptors appears necessary for Methods Ultrasonic calls were recorded in adult male rats spontaneous calling. that were initially screened with amphetamine to eliminate low 50-kHz callers. The remaining subjects were tested after Keywords Vocalization . Dopamine receptor . Reward . acute intraperitoneal or subcutaneous injection of the fol- Aversion . Agonist . Antagonist . Reinforcement . lowing DA receptor-selective agonists and antagonists: Behavior . D1 [D-1] . D2 [D-2] A68930 (D1-like agonist), quinpirole (D2-like agonist), PD 128907 (D3 agonist), PD 168077 (D4 agonist), SCH 39166 (D1-like antagonist), L-741,626 (D2 antagonist), Introduction NGB 2904 (D3 antagonist), and L-745,870 (D4 antagonist). -
Selective Blockade of the Metabotropic Glutamate Receptor Mglur5 Protects Mouse Livers in in Vitro and Ex Vivo Models of Ischemia Reperfusion Injury
International Journal of Molecular Sciences Article Selective Blockade of the Metabotropic Glutamate Receptor mGluR5 Protects Mouse Livers in In Vitro and Ex Vivo Models of Ischemia Reperfusion Injury Andrea Ferrigno 1,* ID , Clarissa Berardo 1, Laura Giuseppina Di Pasqua 1, Veronica Siciliano 1, Plinio Richelmi 1, Ferdinando Nicoletti 2,3 and Mariapia Vairetti 1 ID 1 Department of Internal Medicine and Therapeutics, Cellular and Molecular Pharmacology and Toxicology Unit, University of Pavia, 27100 Pavia, Italy; [email protected] (C.B.); [email protected] (L.G.D.P.); [email protected] (V.S.); [email protected] (P.R.); [email protected] (M.V.) 2 Department of Physiology and Pharmacology, Sapienza University, 00185 Roma, Italy; [email protected] 3 I.R.C.C.S. Neuromed, 86077 Pozzilli, Italy * Correspondence: [email protected]; Tel.: +39-0382-986451 Received: 20 November 2017; Accepted: 22 January 2018; Published: 23 January 2018 Abstract: 2-Methyl-6-(phenylethynyl)pyridine (MPEP), a negative allosteric modulator of the metabotropic glutamate receptor (mGluR) 5, protects hepatocytes from ischemic injury. In astrocytes and microglia, MPEP depletes ATP. These findings seem to be self-contradictory, since ATP depletion is a fundamental stressor in ischemia. This study attempted to reconstruct the mechanism of MPEP-mediated ATP depletion and the consequences of ATP depletion on protection against ischemic injury. We compared the effects of MPEP and other mGluR5 negative modulators on ATP concentration when measured in rat hepatocytes and acellular solutions. We also evaluated the effects of mGluR5 blockade on viability in rat hepatocytes exposed to hypoxia. Furthermore, we studied the effects of MPEP treatment on mouse livers subjected to cold ischemia and warm ischemia reperfusion. -
Sex Differences in Nicotine-Conditioned Hyperactivity in a Model of Dopamine D2 Receptor Priming: Roles of Dopamine D2 and D3 Receptor Subtypes
East Tennessee State University Digital Commons @ East Tennessee State University Electronic Theses and Dissertations Student Works 8-2008 Sex Differences in Nicotine-Conditioned Hyperactivity in a Model of Dopamine D2 Receptor Priming: Roles of Dopamine D2 and D3 Receptor Subtypes. Ashley Brianna Sheppard East Tennessee State University Follow this and additional works at: https://dc.etsu.edu/etd Part of the Hormones, Hormone Substitutes, and Hormone Antagonists Commons Recommended Citation Sheppard, Ashley Brianna, "Sex Differences in Nicotine-Conditioned Hyperactivity in a Model of Dopamine D2 Receptor Priming: Roles of Dopamine D2 and D3 Receptor Subtypes." (2008). Electronic Theses and Dissertations. Paper 1978. https://dc.etsu.edu/etd/ 1978 This Thesis - Open Access is brought to you for free and open access by the Student Works at Digital Commons @ East Tennessee State University. It has been accepted for inclusion in Electronic Theses and Dissertations by an authorized administrator of Digital Commons @ East Tennessee State University. For more information, please contact [email protected]. Sex Differences in Nicotine-conditioned Hyperactivity in a Model of Dopamine D2 Receptor Priming: Roles of Dopamine D2 and D3 Receptor Subtypes A thesis presented to the faculty of the Department of Psychology East Tennessee State University In partial fulfillment of the requirements for the degree of Master of Arts in Psychology by Ashley Brianna Sheppard August 2008 Russell Brown, PhD., Chair Michael Woodruff, PhD., Committee member Otto Zinser, -
Metabotropic Glutamate Receptors
mGluR Metabotropic glutamate receptors mGluR (metabotropic glutamate receptor) is a type of glutamate receptor that are active through an indirect metabotropic process. They are members of thegroup C family of G-protein-coupled receptors, or GPCRs. Like all glutamate receptors, mGluRs bind with glutamate, an amino acid that functions as an excitatoryneurotransmitter. The mGluRs perform a variety of functions in the central and peripheral nervous systems: mGluRs are involved in learning, memory, anxiety, and the perception of pain. mGluRs are found in pre- and postsynaptic neurons in synapses of the hippocampus, cerebellum, and the cerebral cortex, as well as other parts of the brain and in peripheral tissues. Eight different types of mGluRs, labeled mGluR1 to mGluR8, are divided into groups I, II, and III. Receptor types are grouped based on receptor structure and physiological activity. www.MedChemExpress.com 1 mGluR Agonists, Antagonists, Inhibitors, Modulators & Activators (-)-Camphoric acid (1R,2S)-VU0155041 Cat. No.: HY-122808 Cat. No.: HY-14417A (-)-Camphoric acid is the less active enantiomer (1R,2S)-VU0155041, Cis regioisomer of VU0155041, is of Camphoric acid. Camphoric acid stimulates a partial mGluR4 agonist with an EC50 of 2.35 osteoblast differentiation and induces μM. glutamate receptor expression. Camphoric acid also significantly induced the activation of NF-κB and AP-1. Purity: ≥98.0% Purity: ≥98.0% Clinical Data: No Development Reported Clinical Data: No Development Reported Size: 10 mM × 1 mL, 100 mg Size: 10 mM × 1 mL, 5 mg, 10 mg, 25 mg (2R,4R)-APDC (R)-ADX-47273 Cat. No.: HY-102091 Cat. No.: HY-13058B (2R,4R)-APDC is a selective group II metabotropic (R)-ADX-47273 is a potent mGluR5 positive glutamate receptors (mGluRs) agonist. -
GABA Receptors
D Reviews • BIOTREND Reviews • BIOTREND Reviews • BIOTREND Reviews • BIOTREND Reviews Review No.7 / 1-2011 GABA receptors Wolfgang Froestl , CNS & Chemistry Expert, AC Immune SA, PSE Building B - EPFL, CH-1015 Lausanne, Phone: +41 21 693 91 43, FAX: +41 21 693 91 20, E-mail: [email protected] GABA Activation of the GABA A receptor leads to an influx of chloride GABA ( -aminobutyric acid; Figure 1) is the most important and ions and to a hyperpolarization of the membrane. 16 subunits with γ most abundant inhibitory neurotransmitter in the mammalian molecular weights between 50 and 65 kD have been identified brain 1,2 , where it was first discovered in 1950 3-5 . It is a small achiral so far, 6 subunits, 3 subunits, 3 subunits, and the , , α β γ δ ε θ molecule with molecular weight of 103 g/mol and high water solu - and subunits 8,9 . π bility. At 25°C one gram of water can dissolve 1.3 grams of GABA. 2 Such a hydrophilic molecule (log P = -2.13, PSA = 63.3 Å ) cannot In the meantime all GABA A receptor binding sites have been eluci - cross the blood brain barrier. It is produced in the brain by decarb- dated in great detail. The GABA site is located at the interface oxylation of L-glutamic acid by the enzyme glutamic acid decarb- between and subunits. Benzodiazepines interact with subunit α β oxylase (GAD, EC 4.1.1.15). It is a neutral amino acid with pK = combinations ( ) ( ) , which is the most abundant combi - 1 α1 2 β2 2 γ2 4.23 and pK = 10.43. -
Modulators of CXCR4 and CXCR7/ACKR3 Function
Molecular Pharmacology Fast Forward. Published on September 23, 2019 as DOI: 10.1124/mol.119.117663 This article has not been copyedited and formatted. The final version may differ from this version. MOL # 117663 Modulators of CXCR4 and CXCR7/ACKR3 function Ilze Adlere*, Birgit Caspar*, Marta Arimont*, Sebastian Dekkers, Kirsten Visser, Jeffrey Stuijt, Chris de Graaf, Michael Stocks, Barrie Kellam, Stephen Briddon, Maikel Wijtmans, Iwan de Esch, Stephen Hill, Rob Leurs# * These authors contributed equally to this work. Downloaded from # Corresponding author molpharm.aspetjournals.org Griffin Discoveries BV, Amsterdam, The Netherlands (IA, IE, RL), Division of Physiology, Pharmacology and Neuroscience, School of Life Sciences, University of Nottingham, Nottingham, UK (BC, SJB, SJH), Centre of Membrane Proteins and Receptors (COMPARE), Universities of Birmingham and Nottingham, The Midlands, U.K. (BC, BK, SD, SB, SH), at ASPET Journals on September 26, 2021 School of Pharmacy, University of Nottingham, Nottingham, U.K. (SD, BK, MS), Division of Medicinal Chemistry, Amsterdam Institute for Molecules, Medicines and Systems, Faculty of Science, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands (MA, KS, JS, CG, MW, IE, RL), Sosei Heptares, Cambridge, U.K. (CG) 1 Molecular Pharmacology Fast Forward. Published on September 23, 2019 as DOI: 10.1124/mol.119.117663 This article has not been copyedited and formatted. The final version may differ from this version. MOL # 117663 Running title: Modulators of CXCR4 and CXCR7/ACKR3 function Corresponding -
Research in Anxiety Disorders: from the Bench to the Bedside Matthew Garner A,⁎, Hanns Möhler B, Dan J
NEUPSY-10154; No of Pages 10 ARTICLE IN PRESS European Neuropsychopharmacology (2009) xx, xxx–xxx www.elsevier.com/locate/euroneuro REVIEW ARTICLE Research in anxiety disorders: From the bench to the bedside Matthew Garner a,⁎, Hanns Möhler b, Dan J. Stein c, Thomas Mueggler d, David S. Baldwin a a University of Southampton, UK b University of Zurich, Switzerland c University of Cape Town, South Africa d University and ETH of Zurich, Switzerland Received 13 January 2009; accepted 30 January 2009 KEYWORDS Abstract Anxiety; Treatment; The development of ethologically based behavioural animal models has clarified the anxiolytic Imaging; properties of a range of neurotransmitter and neuropeptide receptor agonists and antagonists, Cognition with several models predicting efficacy in human clinical samples. Neuro-cognitive models of human anxiety and findings from fMRI suggest dysfunction in amygdala-prefrontal circuitry underlies biases in emotion activation and regulation. Cognitive and neural mechanisms involved in emotion processing can be manipulated pharmacologically, and research continues to identify genetic polymorphisms and interactions with environmental risk factors that co-vary with anxiety-related behaviour and neuro-cognitive endophenotypes. This paper describes findings from a range of research strategies in anxiety, discussed at the recent ECNP Targeted Expert Meeting on anxiety disorders and anxiolytic drugs. The efficacy of existing pharmacological treatments for anxiety disorders is discussed, with particular reference to drugs modulating serotonergic, noradrenergic and gabaergic mechanisms, and novel targets including glutamate, CCK, NPY, adenosine and AVP. Clinical and neurobiological predictors of active treatment and placebo response are considered. © 2009 Published by Elsevier B.V. Anxiety symptoms are common in the community, and typically persist for many years, and are associated with anxiety disorders are common in primary and secondary significant personal distress, reduced quality of life, medical care settings (King et al., 2008). -
NINDS Custom Collection II
ACACETIN ACEBUTOLOL HYDROCHLORIDE ACECLIDINE HYDROCHLORIDE ACEMETACIN ACETAMINOPHEN ACETAMINOSALOL ACETANILIDE ACETARSOL ACETAZOLAMIDE ACETOHYDROXAMIC ACID ACETRIAZOIC ACID ACETYL TYROSINE ETHYL ESTER ACETYLCARNITINE ACETYLCHOLINE ACETYLCYSTEINE ACETYLGLUCOSAMINE ACETYLGLUTAMIC ACID ACETYL-L-LEUCINE ACETYLPHENYLALANINE ACETYLSEROTONIN ACETYLTRYPTOPHAN ACEXAMIC ACID ACIVICIN ACLACINOMYCIN A1 ACONITINE ACRIFLAVINIUM HYDROCHLORIDE ACRISORCIN ACTINONIN ACYCLOVIR ADENOSINE PHOSPHATE ADENOSINE ADRENALINE BITARTRATE AESCULIN AJMALINE AKLAVINE HYDROCHLORIDE ALANYL-dl-LEUCINE ALANYL-dl-PHENYLALANINE ALAPROCLATE ALBENDAZOLE ALBUTEROL ALEXIDINE HYDROCHLORIDE ALLANTOIN ALLOPURINOL ALMOTRIPTAN ALOIN ALPRENOLOL ALTRETAMINE ALVERINE CITRATE AMANTADINE HYDROCHLORIDE AMBROXOL HYDROCHLORIDE AMCINONIDE AMIKACIN SULFATE AMILORIDE HYDROCHLORIDE 3-AMINOBENZAMIDE gamma-AMINOBUTYRIC ACID AMINOCAPROIC ACID N- (2-AMINOETHYL)-4-CHLOROBENZAMIDE (RO-16-6491) AMINOGLUTETHIMIDE AMINOHIPPURIC ACID AMINOHYDROXYBUTYRIC ACID AMINOLEVULINIC ACID HYDROCHLORIDE AMINOPHENAZONE 3-AMINOPROPANESULPHONIC ACID AMINOPYRIDINE 9-AMINO-1,2,3,4-TETRAHYDROACRIDINE HYDROCHLORIDE AMINOTHIAZOLE AMIODARONE HYDROCHLORIDE AMIPRILOSE AMITRIPTYLINE HYDROCHLORIDE AMLODIPINE BESYLATE AMODIAQUINE DIHYDROCHLORIDE AMOXEPINE AMOXICILLIN AMPICILLIN SODIUM AMPROLIUM AMRINONE AMYGDALIN ANABASAMINE HYDROCHLORIDE ANABASINE HYDROCHLORIDE ANCITABINE HYDROCHLORIDE ANDROSTERONE SODIUM SULFATE ANIRACETAM ANISINDIONE ANISODAMINE ANISOMYCIN ANTAZOLINE PHOSPHATE ANTHRALIN ANTIMYCIN A (A1 shown) ANTIPYRINE APHYLLIC -
Aldrich Raman
Aldrich Raman Library Listing – 14,033 spectra This library represents the most comprehensive collection of FT-Raman spectral references available. It contains many common chemicals found in the Aldrich Handbook of Fine Chemicals. To create the Aldrich Raman Condensed Phase Library, 14,033 compounds found in the Aldrich Collection of FT-IR Spectra Edition II Library were excited with an Nd:YVO4 laser (1064 nm) using laser powers between 400 - 600 mW, measured at the sample. A Thermo FT-Raman spectrometer (with a Ge detector) was used to collect the Raman spectra. The spectra were saved in Raman Shift format. Aldrich Raman Index Compound Name Index Compound Name 4803 ((1R)-(ENDO,ANTI))-(+)-3- 4246 (+)-3-ISOPROPYL-7A- BROMOCAMPHOR-8- SULFONIC METHYLTETRAHYDRO- ACID, AMMONIUM SALT PYRROLO(2,1-B)OXAZOL-5(6H)- 2207 ((1R)-ENDO)-(+)-3- ONE, BROMOCAMPHOR, 98% 12568 (+)-4-CHOLESTEN-3-ONE, 98% 4804 ((1S)-(ENDO,ANTI))-(-)-3- 3774 (+)-5,6-O-CYCLOHEXYLIDENE-L- BROMOCAMPHOR-8- SULFONIC ASCORBIC ACID, 98% ACID, AMMONIUM SALT 11632 (+)-5-BROMO-2'-DEOXYURIDINE, 2208 ((1S)-ENDO)-(-)-3- 97% BROMOCAMPHOR, 98% 11634 (+)-5-FLUORODEOXYURIDINE, 769 ((1S)-ENDO)-(-)-BORNEOL, 99% 98+% 13454 ((2S,3S)-(+)- 11633 (+)-5-IODO-2'-DEOXYURIDINE, 98% BIS(DIPHENYLPHOSPHINO)- 4228 (+)-6-AMINOPENICILLANIC ACID, BUTANE)(N3-ALLYL)PD(II) CL04, 96% 97 8167 (+)-6-METHOXY-ALPHA-METHYL- 10297 ((3- 2- NAPHTHALENEACETIC ACID, DIMETHYLAMINO)PROPYL)TRIPH 98% ENYL- PHOSPHONIUM BROMIDE, 12586 (+)-ANDROSTA-1,4-DIENE-3,17- 99% DIONE, 98% 13458 ((R)-(+)-2,2'- 963 (+)-ARABINOGALACTAN BIS(DIPHENYLPHOSPHINO)-1,1'- -
Bombesin Receptors in Distinct Tissue Compartments of Human Pancreatic Diseases Achim Fleischmann, Ursula Läderach, Helmut Friess, Markus W
0023-6837/00/8012-1807$03.00/0 LABORATORY INVESTIGATION Vol. 80, No. 12, p. 1807, 2000 Copyright © 2000 by The United States and Canadian Academy of Pathology, Inc. Printed in U.S.A. Bombesin Receptors in Distinct Tissue Compartments of Human Pancreatic Diseases Achim Fleischmann, Ursula Läderach, Helmut Friess, Markus W. Buechler, and Jean Claude Reubi Division of Cell Biology and Experimental Cancer Research (AF, UL, JCR), Institute of Pathology, University of Berne, and Department of Visceral and Transplantation Surgery (HF, MWB), Inselspital, University of Berne, Berne, Switzerland SUMMARY: Overexpression of receptors for regulatory peptides in various human diseases is reportedly of clinical interest. Among these peptides, bombesin and gastrin-releasing peptide (GRP) have been shown to play a physiological and pathophysiological role in pancreatic tissues. Our aim has been to localize bombesin receptors in the human diseased pancreas to identify potential clinical applications of bombesin analogs in this tissue. The presence of bombesin receptor subtypes has been evaluated in specimens of human pancreatic tissues with chronic pancreatitis (n ϭ 23) and ductal pancreatic carcinoma (n ϭ 29) with in vitro receptor autoradiography on tissue sections incubated with 125I-[Tyr4]-bombesin or the universal ligand 125I-[D-Tyr6, -Ala11, Phe13, Nle14]-bombesin(6–14) as radioligands and displaced by subtype-selective bombesin receptor agonists and antagonists. GRP receptors were identified in the pancreatic exocrine parenchyma in 17 of 20 cases with chronic pancreatitis. No measurable bombesin receptors were found in the tumor tissue of ductal pancreatic carcinomas, however, GRP receptors were detected in a subset of peritumoral small veins in 19 of 29 samples.